Disease relevance of CDKL2

• To facilitate studies on its induction pattern and cellular functions, we expressed recombinant P56 as a hexahistidine-tagged protein in Escherichia coli and purified it to apparent homogeneity using affinity chromatography [1].
• Cellular expression of P56 by transfection did not inhibit the replication of vesicular stomatitis virus and encephalomyocarditis virus [1].
• Surprisingly, Sendai virus could also induce P56 in the mutant cell line P2.1, which cannot respond to either IFN-alpha/beta or double-stranded RNA [1].
• Characterization of the interaction between the interferon-induced protein P56 and the Int6 protein encoded by a locus of insertion of the mouse mammary tumor virus [2].
• Injection of recombinant human GH (rhGH, 3 mg/kg, twice daily, sc) between postnatal day 14 (P14) to P56 failed to stimulate their growth as measured as both body weight and length [3].

Psychiatry related information on CDKL2

• However, stress-induced locomotor activity was significantly increased in the Caesarean birth plus anoxia at P35, while after puberty (at P56), saline injection, D-amphetamine and stress-induced locomotion were significantly enhanced in the Caesarean birth plus anoxia compared to its control groups [4].

High impact information on CDKL2

• In contrast, wild-type mice receiving the same doses of rhGH exhibited accelerated growth starting at P21 that continued until P56, when their body weight was increased by 30% and length by 12% compared with control mice treated with diluent [3].
• Secreted FZD-related protein-2 (SFRP2), a WNT antagonist, was not detected in the P0 uterus, but was abundant in the aglandular caruncular areas of the endometrium between P7 and P56 [5].
• P56 is the most abundant protein induced by interferon (IFN) treatment of human cells [1].
• P56 synthesis was rapidly induced by IFN-beta, and the protein had a half-life of 6 h [1].
• Induction of P56 in the P2.1 cells and the parental U4C cells by virus infection was preceded by activation of IRF-3 as judged by its translocation to the nucleus from the cytoplasm [1].

Biological context of CDKL2

• [J. Opt. Soc. Am. A 3(13), P56 (1986)] was applied to contrast-sensitivity data from 100 older subjects (ages 53-85 years) [6].
• A perfect TATA Box consensus sequence 30 bp further upstream, which is highly conserved among HPVs associated with cervical cancer, was required for the activity of this novel promoter, denoted here as P56 [7].

Anatomical context of CDKL2

• We detected transcripts initiating from both the P105 and the P56 in primary keratinocytes harboring episomal HPV18 as well as in the HPV 18 positive cervical carcinoma cell lines HeLa, C4-1 and SW756 [7].

Associations of CDKL2 with chemical compounds

• In contrast, the activity responsible for the conversion of P56 into P50 was inhibited by each of the cysteine protease inhibitors E-64, leupeptin and iodoacetoamide [8].

Analytical, diagnostic and therapeutic context of CDKL2

• Molecular cloning of the epidermal growth factor-stimulated protein kinase p56 KKIAMRE [9].
• The P56-P48 interaction was confirmed in human cells by co-immunoprecipitation assays and confocal microscopy [10].
• Gel filtration assays revealed that P56 binds to the large eIF-3 complex that contains P48 [10].
• In contrast, removal of an internal domain of P56 enhanced the interaction, as quantified by the two-hybrid assay [2].
• Caesarean section birth with or without an additional period of anoxia was performed in Sprague-Dawley rats and their behaviors were studied at P35 and P56, respectively [4].

References